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Friday, September 7, 2012

The grand schema things

Even a quick glance at the adjacent picture should bring to
mind for most people not only the name of this famous person, but a whole host
of associated information – what he does (he’s an actor), perhaps some movies
he’s been in, who he’s married to, maybe even who he’s no longer married to.
Most of this information (depending on one’s level of familiarity with the
particulars of the gentleman in question) will have sprung to mind automatically
and effortlessly– indeed, it would be very difficult to actively stop it
springing to mind, once the person is recognised. (Try thinking of an elephant
without thinking of what colour it is).

For some people, however, it is anything but effortless – it
is impossible. Readers with prosopagnosia, for example, may still be waiting to
find out who the hell I’ve been writing about (it’s Brad Pitt). This condition,
also known as face blindness, impairs the ability to recognise people by their
faces – the visual stimulus of the face is not linked in the normal way to the
rest of the associated information. Similarly, people with colour agnosia may
be perfectly able to think of elephants without thinking of the colour grey –
in fact, they might be unable to bring the appropriate colour to mind even if
asked to. In this case, colour is not connected into the wider concepts of
types of objects.

These networks of associations are called “schemas” – the
mental representations of the various attributes of a person, object or
concept. The interesting thing about them is that they link very different
types of information (from the different senses, for example) – information
that is processed in very different parts of the brain. For a schema to emerge
that includes all the relevant information, all the relevant regions of the
brain have to be talking to each other. One hypothesis to explain conditions
like prosopagnosia or colour agnosia is that the face or colour regions of the
brain are not wired into the wider network normally.

Schemas are built up through experience – we learn that bananas
are yellow and curved and about so big and a bit mushy and smell and taste like
banana. Just thinking of a banana will bring many of those attributes to mind
(though, interestingly, usually not the smell or taste, even though smelling or
tasting one can activate the schema). Similarly, we learn that the letter “A”
looks like that, or like this: “a” or this: “a” or this: “a” and makes a sound like “ay”
or “ah” or the way New Zealanders pronounce it, which cannot be written down.

This kind of learning is believed to involve strengthening
connections between ensembles of neurons that represent the various attributes
of an object (or type of object). If these various attributes reliably occur
together, then the connections between these representations are strengthened.
So much so, that activating the representation of one of the attributes of an
object (like the shape of the letter A) is usually enough to cross-activate the
representations of its other attributes (such as its canonical sounds).

Schemas are thus the neural substrates of knowledge – the
statistical regularities and contingencies of our experience wired into our
neural networks. The conditions referred to as “agnosias” – literally the lack
of knowledge of something – can generally be thought of as a failure to link
all the attributes of an object into a schema. These include the conditions
mentioned above, but also other types of object agnosia (which are quite
diverse and sometimes bizarrely specific), as well as things like congenital amusia (also known as tone or tune deafness) and dyslexia and dyscalculia.

Agnosias can be acquired – usually caused by injury to
specific parts of the brain. But there is a growing appreciation that they can
also be congenital, and, in some cases, are very clearly inherited in what
seems like a Mendelian manner. These conditions are also not as rare as one
might expect – face blindness may affect 1-2% of the population, for example.
Familial inheritance of this condition, as well as congenital amusia and colour
agnosia have all been documented and the high heritability of dyslexia and
dyscalculia is well known.

Specific mutations may thus cause an inability to link faces
to other information about people, or to link the sounds and shapes of letters,
or to link colour to the rest of our knowledge about objects. This may sound
like a paradox – after all, I have just been saying that the development of
these schemas depends on experience. That is true, but the ability to link different
attributes together depends on the wiring of the brain, which can be affected
by genetic mutations. If the different regions of the brain are not connected
normally then the opportunity for experience to link contingent stimuli will
not arise.

There is evidence of physical differences in connectivity in
the brains of people with some of these conditions, particularly between
regions processing the various stimuli. These conditions may also be
characterised by not only a disconnection between various elements of a network
– which represent various attributes of an object – but by a further disconnection between these networks and frontal areas that mediate conscious
awareness.

There is good evidence in prosopagnosia, for example, that
faces of familiar people are actually “recognised” by visual brain areas (which
show a different response than to strange faces), even though the person is
unaware of this recognition. Similar results have been reported for congenital
amusia, where discordant notes are detected by the brain, but not reported to the mind of the person.

If these disorders can be thought of as “disconnection
syndromes”, the condition of synaesthesia may reflect just the opposite –
hyperconnectivity between brain areas. This condition is usually thought of as
a cross-sensory phenomenon – a triggering of visual percepts by sounds, for
example, or the experience of tactile shapes triggered by tastes. In many
cases, however, the triggers and the induced experiences are not sensory, but
cognitive – the automatic association, conceptually, of some extra attribute
into the schema of an object. This extra attribute may or may not be actively
experienced as a percept.

For example, a common experience in synaesthesia is having a
coloured alphabet, where different letters “have” different colours. These
associations are highly idiosyncratic but also very stable and very definite –
the colour of a particular letter is as much an integral part of its schema for
that person as the shapes and sounds associated with it. Similarly, the shape
of a taste or the taste of a word, the smell of a musical note or the
personality of a number – these are all extra attributes integrally tied to the
larger concepts of the inducing stimuli.

Like many agnosias, synaesthesia runs very strongly in families and most are characterised by an apparently simple mode of
inheritance. It is quite common for different members of a family to have
different types of synaesthetic experiences, however. This suggests that a
general predisposition to the condition can be inherited, but that the
particular form that emerges depends on additional factors, possibly including
chance variation in brain development as well as experience.

One hypothesis to explain synaesthesia is that genetic
differences affect the wiring of networks of brain areas, resulting in this
case in the inclusion of extra areas into networks to which they do not
normally belong. An initial difference in wiring may then alter the subjective
experience of the person as they are learning to recognise and categorise
various types of stimuli (such as letters, numbers, musical notes, flavours,
etc.). If, for example, the “colour area(s)” of the brain are reliably co-activated
when letters are being learned, then the experienced colour will be
automatically incorporated into the schema of each letter.

We do not yet know the identity of any of the affected genes
in these conditions, (with a couple exceptions for dyslexia), but it is likely
they will be discovered in the near future. It is important to note that these
will not be genes “for reading” or “for face processing” or “for not thinking
letters have colours”. Their normal functions may be far removed from the
effects when they are mutated. For example, one gene known to result in a
condition characterised by dyslexia encodes a protein required for normal cell migration. Altered neuronal migration leads to groups of ectopic neurons
located in the white matter of the brain – these are thought to impair
communication along these nerve fibres, resulting in disconnection of areas
required for linking the visual shapes of graphemes with their associated
phonemes (that’s the working hypothesis at least). This is a gene for neuronal
migration, not for reading.

But the identification of genes involved in these conditions
will tell us a lot about an area of developmental neurobiology we still know
very little about – how different areas of the cerebral cortex become, on the
one hand, specialised to process specific types of information and, on the
other, integrated into larger networks that allow different aspects to be associated
through experience. This relies on both the initial wiring of cortical
networks, driven by a genetic program, and their subsequent refinement as we learn
that elephants are grey, bananas are mushy and Brad Pitt is one lucky
son-of-a-bitch.

11 comments:

Still one of the best books on this topic is Rethinking Innateness by Elman et al (1996). It would be interesting to go back and flesh out the (pretty abstract) ideas in that book with everything we've learnt since about genetics and the brain.

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I have only just come across this interesting blog, as I have just become a blogger myself, and was doing a google blog search on those subjects that interest me. I have an interest these days, thanks to having the magic of internet available in these, my golden years.. in finding out everything I can in relation to various aspects of what makes the human brain "tick", and I do find some subjects more interesting than others in this regard. In particular there are 2 things which I seek (from credible sources) info on - in regard to the way the brain is "wired".

Firstly, ever since I first realised about 10 years ago that there actually was such a thing as "face-blindness", I am so much more comfortable with this affliction now that I know it DOES exist, although I have never asked for a diagnosis from any doctor. (Felt too silly!) I know these days that all of my life I have had this, and never found out it was an actual anomoly of the brain until I first saw it described on the internet about 10 years ago! This condition I now know, did have some effect on my early development I am quite sure in hindsight.. but at least now I understand why. Unless one actually experiences this phenomenom, this is a frustrating condition to say the least, and can lead to misconceptions by others at its worst!

Other thing is, it was discovered only about 10 years ago also that I have Cavus Septum Pellucidum during a brain scan (I requested the scan out of frustration, as I do suffer anxiety and had taken medication for it for years, and could only describe this feeling to medics and psychologists as being at its worst when my brain "misfired". All this ever brought from these educated people was funny looks!) so I requested the scan! Even as I write, I have discovered that so little is known about the potential effects of CSP in one's life or if indeed there are any. The jury seems to be out on that one. However, I am sure this "dis-connected" feeling (anxiety) is somehow related to the CSP, but I dont think this particular theory has ever been tested properly.

And please dont suggest (however well-meaning you intend to be), CBT, relaxation music, or candles, been there and done all that! Love to get other thoughts on my post though. Cheers

Brad Pitt? Ok, I'll take your word for it.Guess I'm among the lucky 1 to 2%. I'm pretty sure my brother is similarly afflicted.I lived 60 years with the condition without fully understanding why others were so good at something I seemingly can't do. Is anyone collecting DNA to study face blindness. I'd be glad to contribute some spit ;-)

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